ArticleExperimental & molecular medicine2022
O-GlcNAc transferase regulates intervertebral disc degeneration by targeting FAM134B-mediated ER-phagy.
Article in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- ER-phagy receptors: structural mechanisms in selective ER degradation and disease implications.Acta pharmacologica Sinica · 2026Review
- O-GlcNAcylation: A bridge for regulating the function of the "heart-kidney-bone axis".Biochemistry and biophysics reports · 2026Review
- Unveiling ER-Phagy Receptors in Thyroid Cancer: A Combined Approach of Public Data Mining and In Vitro Validation.Clinical Medicine Insights. Oncology · 2026Article
- Astragalus Polysaccharide Enhances O-GlcNAcylation Through OGT to Improve Intervertebral Disc Degeneration in Rats.Journal of cellular and molecular medicine · 2025Article
- From molecular regulation to tissue repair: hydrogels in the fight against intervertebral disc degeneration.Annals of medicine · 2025Review
- Utilising bioinformatics and molecular docking technology to explore the underlying mechanisms of intervertebral disc degeneration with potential therapeutic drugs and formulas.Journal of global health · 2025Article
- Astragalus Polysaccharides Alleviate Lumbar Disc Herniation by Promoting the O-GlcNAcylation of NRF2.Applied biochemistry and biotechnology · 2025Article
- Endoplasmic reticulum-mitochondria coupling prompts ZBP1-mediated RPE cell PANoptosis in age-related macular degeneration.Communications biology · 2025Article
- RBX1 mitigates ferroptosis by inhibiting NCOA4-mediated ferritinophagy and contributes to the attenuation of intervertebral disc degeneration.Journal of translational medicine · 2025Article
- CKAP4 in hepatocellular carcinoma: competitive RETREG1/FAM134B binding, reticulophagy regulation, and cancer progression.Autophagy · 2025Article
- O-GlcNAcylation: Sagacious Orchestrator of Bone-, Joint-, and Spine-Related Diseases.Journal of proteome research · 2025Review
- FAM134B in Cellular Homeostasis: Bridging Endoplasmic Reticulum-Phagy to Human Diseases.International journal of biological sciences · 2025Review
- Exploring Negative Feedback Mechanisms in the PTEN-ACE Axis: Application of Electrosorb Hydrogel-Based Gene Delivery for Intervertebral Disc Regeneration.International journal of biological sciences · 2025Article
- Organellar quality control crosstalk in aging-related disease: Innovation to pave the way.Aging cell · 2025Review
- Integrating Bulk RNA and Single-Cell RNA Sequencing Identifies and Validates Lactylation-Related Signatures for Intervertebral Disc Degeneration.Journal of cellular and molecular medicine · 2024Article
- LTF ameliorates cartilage endplate degeneration by suppressing calcification, senescence and matrix degradation through the JAK2/STAT3 pathway.Journal of cellular and molecular medicine · 2024Article
- O-GlcNAcylation: roles and potential therapeutic target for bone pathophysiology.Cell communication and signaling : CCS · 2024Review
- Glutamine suppresses senescence and promotes autophagy through glycolysis inhibition-mediated AMPKα lactylation in intervertebral disc degeneration.Communications biology · 2024Article
- SSR1 and CKAP4 as potential biomarkers for intervertebral disc degeneration based on integrated bioinformatics analysis.JOR spine · 2024Article
- The role of O-GlcNAcylation in bone metabolic diseases.Frontiers in physiology · 2024Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both O-linked β-N-acetylglucosaminylation (O-GlcNAcylation) and endoplasmic reticulum-phagy (ER-phagy) are well-characterized conserved adaptive regulatory mechanisms that maintain cellular homeostasis and function in response to various stress conditions. Abnormalities in O-GlcNAcylation and ER-phagy have been documented in a wide variety of human pathologies. However, whether O-GlcNAcylation or ER-phagy is involved in the pathogenesis of intervertebral disc degeneration (IDD) is largely unknown. In this study, we investigated the function of O-GlcNAcylation and ER-phagy and the related underlying mechanisms in IDD. We found that the expression profiles of O-GlcNAcylation and O-GlcNAc transferase (OGT) were notably increased in degenerated NP tissues and nutrient-deprived nucleus pulposus (NP) cells. By modulating the O-GlcNAc level through genetic manipulation and specific pharmacological intervention, we revealed that increasing O-GlcNAcylation abundance substantially enhanced cell function and facilitated cell survival under nutrient deprivation (ND) conditions. Moreover, FAM134B-mediated ER-phagy activation was regulated by O-GlcNAcylation, and suppression of ER-phagy by FAM134B knockdown considerably counteracted the protective effects of amplified O-GlcNAcylation. Mechanistically, FAM134B was determined to be a potential target of OGT, and O-GlcNAcylation of FAM134B notably reduced FAM134B ubiquitination-mediated degradation. Correspondingly, the protection conferred by modulating O-GlcNAcylation homeostasis was verified in a rat IDD model. Our data demonstrated that OGT directly associates with and stabilizes FAM134B and subsequently enhances FAM134B-mediated ER-phagy to enhance the adaptive capability of cells in response to nutrient deficiency. These findings may provide a new option for O-GlcNAcylation-based therapeutics in IDD prevention.
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